The control of breathing is essential for life. Without an adequate response to increased carbon dioxide levels, people can suffer from breathing disturbances, sickness, and panic, researchers said.
In worst-case scenarios, it can lead to premature death, as in sudden infant death syndrome, they said.
Researchers from Karolinska Institutet in Sweden conducted a study in mice and found that when exposed to decreased oxygen or increased carbon dioxide levels, the brain releases a small molecule called Prostaglandin E2 (PGE2) to help protect itself and regulate breathing.
The slice contained an arrangement of nerve and supporting cells that allowed it to 'breathe' for three weeks. During this time, researchers monitored the cells and their behaviour in response to changes in the environment.
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"Our novel brainstem culture first revealed that cells responsible for breathing operate in a small-world network. Groups of these cells work very closely with each other, with each group interconnected by a few additional cells that appear to work as hubs," said David Forsberg from Karolinska.
Researchers saw that exposure to different substances made the brainstem breathe faster or slower.
"Perhaps most interesting was its response to carbon dioxide, which triggered a release of PGE2. Here, PGE2 acted as a signalling molecule that increased breathing activity in the carbon dioxide-sensitive brainstem region, leading to slower and deeper breaths, or 'sighs,' said Forsberg.
These new insights have important implications for babies, who experience significantly reduced levels of oxygen during birth, researchers said.
"Our findings go some way to explaining how and why our breathing responses to imbalanced oxygen and carbon dioxide levels are impaired during infectious episodes," said Eric Herlenius from Karolinska.
"It also helps further our understanding of why infection can inhibit breathing so severely in new-born babies," he said.
The findings were published in the journal eLife.